Description
Single cell transcriptomes of 27 IPF, 13 COPD and 14 control lungs were established. Cells were clustered into major cell types, then the immune cells consisting of 116,057 myeloid, 4,742 B-, and 19,165 T-& NK-cells were analyzed and subclustered. Subclustering revealed IPF-associated unique gene expression profiles subpopulations that were specific to the IPF lung. For example, we could identify an IPF-specific macrophage subpopulation which showed a pro-fibrotic profile characterized by SPP1, CHIT1, CCL18, SPARC, LGMN, CTSK, and MMP9 gene expression. Antagonistically, NK- and cytotoxic T-cells revealed a significantly increased expression of the protease inhibitors A2M and PZP in the IPF lung
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Discovering the Immune Cell Landscape in IPF by Whole Lung Single Cell Transcriptomics
Single cell transcriptomes of 27 IPF, 13 COPD and 14 control lungs were established. Cells were clustered into major cell types, then the immune cells consisting of 116,057 myeloid, 4,742 B-, and 19,165 T-& NK-cells were analyzed and subclustered. Subclustering revealed IPF-associated unique gene expression profiles subpopulations that were specific to the IPF lung. For example, we could identify an IPF-specific macrophage subpopulation which showed a pro-fibrotic profile characterized by SPP1, CHIT1, CCL18, SPARC, LGMN, CTSK, and MMP9 gene expression. Antagonistically, NK- and cytotoxic T-cells revealed a significantly increased expression of the protease inhibitors A2M and PZP in the IPF lung